How often you assess the success of Primary PCI with degree of ST segment regression or resolution ?

I posed this query to a freshly hatched , Intelligent and energetic cardiologist in an upscale dedicated heart care center.

He said, “No, we don’t .We always go with TIMI flow in IRA .TIMI 3 flow with less than 30% narrowing of IRA is success, that’s it ! He continued ,very often ,we don’t even Insist to take serial ECGs after the procedure . . . forget about analysing ST segment ! His body language seemed to suggest, he didn’t expect such a question (Silly !) from me , talking about ECG in this era of hyper Interventionism where we literally live within the coronary artery !

What a grave error in coronary cognition ? . . . thats commited day in day out of cath lab all over the globe !

TIMI flows across IRA lesion tell more about epicardial patency while the humble ECG reveals the true myocardial reperfusion.

So ,which will you use for assessment for successful reperfusion ? Ideally both , right !

But , as of 2017 ST segment regression is not considered worthy to define success of pPCI by the all powerful world scientific cardiology community .This is unfortunate (Or Intentional ?) we have ignored this Inspite periodic research papers showing the importance of the same. (Link to this land mark Brodie BR AJC 2005)

Do you know , none of the trials that celebrated the superiority of primary PCI in the last two decades used ST segment criteria. But then ,we realised much later even TIMI 3 flow can have near zero myocardial perfusion.So ,can we now say all these trials are invalid ?

We also never bothered to include no reflow as a liability during pPCI. We have enough data to say even restored No reflow during pPCI has worrying long-term outcome as reocclusion and tissue level perfusion is dismal .(Can we call it a pPCI failure equivalent ?) This is because the Cocktail of anti no-reflow drug we administer often give us a momentary satisfaction with transient myocardial blushes ! (Only to occlude minutes later as the patient is wheeled out of cath lab .We will never ever know how often this happens !) This is because , microvascular bed integrity is notoriously unpredictable and defies the conventional salvage time window . We have seen patients with ultrafast pPCI ending up with severe LV dysfunction.

Final message

If you apply the ST regression criteria by 90* minutes after pPCI (as we do for lysis ) the true success rate of pPCI will emerge .My prediction would be , if you do that routinely the hype of perceived superiority of pPCI might go down the drain (At Least in all low risk STEMI ! ) Let us do a large-scale trial comparing ST regression with TIMI flows, blushes ,frame counts etc and rediscover the true face of our beleaguered coronary microcirculatory sense !

*In fact ST regression should occur much early with pPCI than lysis (May be 10 minutes after restoring IRA patency ! )

Post-ample and a Quiz !

If coronary thrombus laden IRA is the chief culprit in STEMI battle field , Why is that Immediate , routine aspiration of thrombus in the ground zero is counter productive ?

That’s what the sophisticated mega trials of coronary thrombus TASTE, TOTAL revealed. I’m looking for an answer !

Surprisingly , a Danish(DANAMI) study showed ST regression may not be Important in pPCI .This appears curious , especially when it suggests , ST segment regression didn’t occur because of more complete revascularisation by PCI !

Experience would tell us only about 70-80 % of STEMI are truly eligible for a good quality pPCI .(Multivessel CAD, Complex bifurcation lesion, difficulty in identifying IRA, No IRA-sapsms , complete spontaneous reperfusion ) The remaining 20-30 % should , logically be included in the failed pPCI category .This fact is largely concealed in the literature .

Bewareof huge thrombus load in every patient with STEMI .The contribution of mechanical occlusion vs thrombus (in the total occlusion ) is the single mostimportant factor in determining the intervention strategy.

Deploying a stent in a poorly prepared (debrided of thrombus ) lesion confers further continuous risk of a STEMI .Stents smartly jail even large thrombus against the coronary vessels and they release it into the lumen in a controlled fashion and prolong the acute coronary risk phases

If thrombus aspiration does a neat job and establishes a good flow , if the lumen appear good , think twice or even thricebefore deploying a stent .It is akin to stent a zero %lesion and we know it is foolish to do that at any stretch of imagination .(Stenting has never been proven to convert a vulnerable ulcerated lesion into stable one )

IVUS, OCT are not the answer in the above situations as we are dealing with emergency coronary fire fighting !

Of course the intensive anti-platelet protocols , will take care of potential after effectsof the intra coronary contact sport we play ! . But . . . there is a limit for every thing. So spend as little time as possible when attempting catheter based reperfusion during STEMI.

Thrombus spill over to adjacent branch or A mid LAD lesion with stagnating thrombus extending to LCX ostium mimicking two IRA

A bifurcation lesion with both LAD and LCX ostial occlusion.

Multiple active looking plaques with thrombus

STEMI in patients with preexisting CAD . Is it a CTO ? ATO ? (Acute total occlusion ) A CTO ,which is fed by collaterals from contralateral artery , if this feeding vessel is occluded even partially , STEMI will occur in CTO territory . Here , for rapid salvage you need to open the vessel that feeds the CTO territory.

Post CABG and post PCI form a special subset . Some times it is very difficult or even impossible to label a graft as an IRA

Finally and most importantly , when there is no visible lesion in any of the coronary arteries and look near normal ! Is that no IRA ? or Wrong diagnosis of STEMI ? Every one blinks in cath lab . The consultant howls the fellow to verify the ECG . Finally it may well turn out to be an early repolarisation syndrome . These are wages we often pay for the modernity !

How to approach the situation when one is confused with identifying the IRA ?

The good old ECG will come to our rescue sometimes. Realise in a multivessel CAD , ECG is also vested with errors.

Most confusions occur between LAD and diagonal /LCX as there can be a huge overlap in the ECG territory anterolateral segments

In a infero posterior STEMI, if you have both RCA / LCX lesion and you wonder which is the IRA it is easy to solve by looking for RV involvement. (LCX lesions however dominant they are . 99/100 times can not infarct the RV significantly !)

If the lesion is in PDA the issue is made simple.

Doing a primary PCI blindly without knowing the IRA

This is modern-day cardiology at its scientific low ! . Cardiologists indulge in such things much more commonly than one would imagine.

Probably they would reason , it is safe to stent every vessel that is potentiality an IRA , rather than missing it. Though the concept of multivessel stenting in STEMI may help patients with complicated MI , like pump failure , it generally increases risk of primary PCI outcome in otherwise stable STEMI. Primary PCI procedure must be as short as possible. The other option is to do plain balloon angioplasty in less deserving vessels.

Important considerations in the setting of complex multivessel CAD during pPCI .

Fall back on medical therapy

Staged PCI

Deferred or Immediate CABG

Hybrid procedures like PCI with CABG

Final message

IRA identification can indeed be a difficult task during primary PCI. Sound knowledge and experience about coronary anatomy and its draining territories especially in the setting of multivessel CAD is essential to avoid errors.